Technical Abstract:
The objective of this study was to examine effects of feeding Lactobacillus acidophilus strain NP51 to mice challenged with Mycobacterium avium subspecies paratuberculosis (MAP), the causative agent of Johne’s disease. We hypothesized that feeding NP51 would increase Th-1 responses and decrease progression of MAP infection in mice. Thus, Balb/c mice were randomized to treatment groups in a factorial design including mice either fed heat-killed or viable NP51and challenged with either heat-killed or viable MAP. Mice were fed 1 × 10**6 CFU of either heat-killed or viable NP51· mice-1 · day-1 along with normal mouse chow until the end of the study. On day 45, mice were challenged with 1 × 10**8 CFU of heat-killed or viable MAP injected intraperitonealy. Ten mice from each group were euthanized on days 45, 90, 135, and 180. At each sampling period, tissues were excised from mice and cultured for MAP. Splenocytes were cultured in vitro with either MAP antigen or concanavalin A and examined for proliferation of T cells subpopulations. Overall, feeding NP51 to mice (either heat-killed or viable) significantly increased the frequency of CD8+ cytotoxic T cells in spleens of mice infected with viable MAP. Most importantly, MAP burden was decreased in the mesenteric lymph nodes, livers, and spleens of mice fed the NP51 compared with the MAP-infected controls on day 135. These results suggest that feeding NP51 modifies the immune responses and prevents progression of MAP infection in Balb/c in mice.
Key words: MAP, NP51, Johne’s disease.
Supported in part by the Nutrition Physiology Corp.